小眼畸形相关转录因子
PI3K/AKT/mTOR通路
MAPK/ERK通路
蛋白激酶B
癌症研究
蛋白激酶A
激酶
生物
转录因子
信号转导
细胞生物学
医学
生物化学
基因
作者
Yijun Li,Shanshan Yuan,Jiaming Liu,Yu Wang,Yanting Zhang,Xiaolu Chen,Wangli Si
摘要
Abstract Human chromosomal segregation 1‐like (CSE1L) gene functions as a key molecular mediator in cellular proliferation, invasion, and apoptosis. The association of CSE1L with tumor progression has been reported in diverse human cancers. A greater understanding of CSE1L molecular mechanism is beneficial for cancer treatment. In the current study, we show that CSE1L was highly expressed in gastric cancer (GC) cell lines. CSE1L silence promoted apoptosis and inhibited cell proliferation and invasion. Overexpression of glycoprotein nonmetastatic melanoma protein B (GPNMB) reversed the anticancer effect of CSE1L inhibition. CSE1L inhibition decreased GPNMB by microphthalmia‐associated transcription factor (MITF). Moreover, GPNMB regulates the phosphoinositide 3‐kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR) and mitogen‐activated protein kinase kinase (MEK)/extracellular signal‐regulated kinase (ERK) signaling pathway. Taken together, our study revealed that CSE1L inhibition decreased MITF and suppressed GPNMB expression, thereby activating the PI3K/Akt/mTOR and MEK/ERK signaling pathway, ultimately inhibiting the tumor growth and metastasis in GC.
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